Abstract
The frequency of miniature excitatory postsynaptic currents (mEPSCs) in cultured hippocampal neurons increases under the action of drugs that trigger a rise in the intracellular concentration of cyclicAMP. It is generally believed that this type of effect is mediated by protein kinase A. Here, we show that it largely depends on the activation of hyperpolarization-activated cation channels (Ih) by cyclicAMP. In mammals, Ih channels control membrane excitability, thanks to their function as ionic channels. Here, we show that the effect of Ih channels on glutamate release is not mediated by the depolarization induced by their activation and thus is not linked to the ionic channel aspect of Ih channels. This suggests that the Ih channel could be a bifunctional protein.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
